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Genome evolution
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Evan Eichler
University of Washington, US
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Evan Eichler is a Professor and Howard Hughes Medical Institute Investigator in the Department of Genome Sciences, University of Washington School of Medicine, US. He graduated with a B.Sc. Honours degree in Biology from the University of Saskatchewan, CA in 1990. He received his PhD. in 1995 from the Department of Molecular and Human Genetics at Baylor College of Medicine, Houston. After a Hollaender post-doctoral fellowship at Lawrence Livermore National Laboratory, he joined the faculty of Case Western Reserve University in 1997 and later the Department of Genome Sciences in 2004. He was a March of Dimes Basil O'Connor Scholar (1998-2001), was appointed as an HHMI Investigator (2005), and awarded an AAAS Fellowship (2006) and the American Society of Human Genetics Curt Stern Award (2008). He is an editor of Genome Research and has served on various scientific advisory boards for both NIH and NSF. His research group provided the first genome-wide view of segmental duplications within human and other primate genomes and he is a leader in an effort to identify and sequence normal and disease-causing structural variation in the human genome. The long-term goal of his research is to understand the evolution and mechanisms of recent gene duplication and its relationship to copy-number variation and human disease.
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Title & synopsis
Human genome structural variation, disease & evolution
Structural variation of the genome is an important aspect in our understanding of human disease and evolution. I will focus on the genome-wide discovery, analysis and distribution of copy-number and structural variants within the "normal" human population with a particular emphasis on resolving these events at the single basepair level. I will summarize data from a project to catalogue all structural variation from the genomes of nine normal individuals using a clone-based sequence approach. I will present data showing how common structural polymorphisms may predispose to genetic disease and how historical hotspots of variation can be used to identify previously undescribed microdeletion and microduplication syndromes associated with various forms of pediatric disease including mental retardation, epilepsy, diabetes and renal disease. I will present these differences in the context of the evolution of our genome and provide examples of how these regions simultaneously predispose to disease as well as being potentially adaptive during human genome evolution. The challenges and importance of resolving historical and contemporary structural variation will be discussed.
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 Jeffrey Bennetzen
University of Georgia, US
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Jeff Bennetzen received his PhD in Biochemistry from the University of Washington (Seattle, US) in 1980. He joined the Department of Biological Sciences at Purdue University as an Assistant Professor in 1983. Since 2003, he has been the Giles Professor of Molecular Biology & Functional Genomics in the Department of Genetics at the University of Georgia, US, and is currently Department Head. He was elected a member of the US National Academy of Sciences in 2004 and as a Fellow of the American Association for the Advancement of Science in 2005. His other awards include the Sigma Xi Research Award (1995) and Umbarger Professorship (1999) from Purdue University, the Nehru Centenary Professorship from the University of Hyderabad (2002), a Georgia Research Alliance Professorship (2003), and a Guggenheim Fellowship (2008). The Bennetzen laboratory has spent nearly 30 years investigating the factors responsible for the very rapid evolution of higher plant genomes. |
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Title & synopsis
Hyperevolution of flowering plant genomes Flowering plant genomes change rapidly due to frequent polyploidy, recurrent bouts of transposable element activity and aggressive processes for DNA removal. None of this change is randomly distributed in either genome location or lineage of occurrence. These dynamic processes create a hyperevolving genome that is dramatically resistant to functional change, with some notable exceptions.
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Paul Rainey
Massey University, NZ & Max Planck Institute, Plön, DE
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Paul Rainey Paul Rainey is professor of evolutionary genetics and James Cook Research Fellow at the New Zealand Institute for Advanced Study, Massey University at Albany. He is also a Member of the Max Planck Society and External Scientific Member (Honorary Director) at the Max Planck Institute for Evolutionary Biology in Plön, Germany; visiting professor at Stanford, where he is co-director of the Hopkins Microbial Diversity Programme, Principle Investigator at the Allan Wilson Centre for Molecular Ecology & Evolution, and a Fellow of the Royal Society of New Zealand. He completed his PhD at the University of Canterbury in 1989 and moved to Cambridge where he worked as a post doctoral fellow. In 1994 he received a BBSRC Advanced Research Fellowship, which he took to the Department of Plant Sciences at the University of Oxford. In 1996 he was appointed to a faculty position at Oxford, a fellowship at St Cross College, and a stipendiary lectureship at Wadham. With much dedication, he also ran his college's wine cellar. In 2003 he returned to New Zealand as Chair of Ecology and Evolution at the University of Auckland, but retained a fractional professorial position at Oxford until the end of 2005. In 2007 he moved his lab to Massey University's Albany campus. His research focuses on evolutionary process with interests that span several hierarchical levels, from genes (and proteins), chromosomes, cells, kin-groups through to ecosystems. His work is both theoretical and empirical and makes use of microbial populations in order to observe and dissect evolution in real time. A growing fascination is the evolutionary origins of multicellularity, and the role of development in evolution. Other interests include the ecological significance of diversity in natural microbial populations; evolutionary processes determining patterns of diversity in space and time; the origins of selfish genetic elements, and the genetics and fitness consequences of traits that enhance ecological performance in populations of plant-colonizing bacteria. |
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Title & synopsis
Bottlenecks, exclusion rules & the evolutionary genetics of bet-hedging Bet-hedging - stochastic switching between phenotypic states - is a canonical example of an evolutionary adaptation that facilitates persistence in the face of fluctuating environmental conditions. I will describe experiments using bacterial populations in which bet hedging types evolved de novo during the course of selection. Drawing upon findings from genetics and genome resequencing I will outline the series of mutations (and their phenotypic effects) that underpinned the emergence of the bet hedging types. I will give particular attention to the final mutation, which established a bi-stable (epigenetic) switch.
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Michael Stratton
Sanger Centre, UK
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Michael Stratton is Director of the Wellcome Trust Sanger Institute, UK. He qualified in medicine at Oxford University and Guy's Hospital, obtained a PhD in the molecular biology of cancer at the Institute of Cancer Research, London and trained as a histopathologist. His primary research interests have been in the genetics of cancer. He mapped to chromosome 13 and identified the high risk breast cancer susceptibility gene BRCA2, has subsequently identified moderate risk breast cancer susceptibility genes including CHEK2, ATM, BRIP1 and PALB2 and characterised the histopathological features of breast cancers in individuals carrying susceptibility alleles. He identified the gene for hereditary cylindromatosis, a highly disfiguring predisposition to adnexal skin tumours, as well as susceptibility genes for testis, colorectal, thyroid, and childhood cancers. In 2000 he initiated the Cancer Genome Project at the Wellcome Trust Sanger Institute which conducts high throughput, systematic genome-wide searches for somatic mutations in human cancer. The primary aims of this work are to identify new cancer genes, to understand processes of mutagenesis and to reveal the role of genome structure in determining abnormalities of cancer genomes. Through these studies he discovered mutations in the BRAF gene in malignant melanoma, mutations of the ERBB2 gene in lung cancer, and mutations of histone methylases and demethylases in renal and other cancers. He has described the basic patterns of somatic mutation in cancer genomes and used next generation sequencing to generate catalogues of somatic mutations in cancer genomes. |
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Title & synopsis
Evolution of the cancer genome
All cancers carry somatically acquired changes in their genomes. Some, termed "driver" mutations, are causally implicated in cancer development. The remainder are "passengers", and bear the imprints of mutational processes operative during cancer development. Following the advent of second generation sequencing technologies the provision of whole cancer genome sequences has become a reality. These sequences generate comprehensive catalogues of somatic mutations, including point mutations, rearrangements and copy number changes and provide insights into the evolutionary processes underlying the development of individual human cancers including the factors generating variation and the forces of selection. These insights will form the foundation of our understanding of cancer causation, prevention and treatment in the future.
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Hosts & microbes
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Paul Schulze-Lefert
Max Planck Institute, Cologne, DE
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Paul Schulze-Lefert is the Head of Department of Plant Microbe Interactions at the Max-Planck-Institute for Plant Breeding Research, Cologne, DE. He was trained in biochemistry and genetics at Marburg, Freiburg, and Cologne Universities, DE. Major research areas are the innate immune system of plants, mechanisms of fungal pathogenesis, the molecular basis of biotrophic lifestyle, and functional studies on the plant microbiome. His research activities include the development of quantitative non-invasive imaging techniques to better understand the dynamic nature of immune responses at subcellular resolution. Much of his current work is dedicated to bridging traditional research areas like genetics, biochemistry, and cell biology in the endeavor of increasing our understanding of the molecular mechanisms that control plant microbe interactions. He is an elected EMBO member since April 2006, an elected member of the National Academy of Sciences, US, and the "Deutsche Akademie der Naturforscher Leopoldina",DE.
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Title & synopsis
From plant-pathogen interactions to plant-microbe communities
Current concepts of the plant innate immune system are largely based on two forms of immunity that engage distinct classes of immune receptors. The existence of this elaborate immune system creates a potential paradox: how then can plants serve in nature as hosts of a staggering diversity of commensalistic and mutualistic microorganisms throughout their life cycle? I will present our approaches to survey the Arabidopsis microbiome and discuss whether host determinants shape plant-associated bacterial communities in the rhizosphere. |
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Lucy Shapiro
Stanford University, US
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Lucy Shapiro is a Professor in the Department of Developmental Biology at Stanford University School of Medicine where she holds the Virginia and D. K. Ludwig Chair in Cancer Research and is the Director of the Beckman Center for Molecular and Genetic Medicine. She is a member of the Board of Advisors of The Pasteur Institute, the Ludwig Institute for Cancer Research, and the US Lawrence Berkeley National Labs. She founded the anti-infectives discovery company, Anacor Pharmaceuticals and is a member of the Anacor Board of Directors. Professor Shapiro has been the recipient of multiple honors, including: election to the American Academy of Arts and Sciences, the US National Academy of Sciences, and the American Philosophical Society. She was awarded the 2005 Selman Waksman Award from the National Academy of Sciences, the Canadian International 2009 Gairdner Award, the 2009 John Scott Award, and the 2010 Abbott Lifetime Achievement Award. |
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Title & synopsis
The Systems Architecture of the Bacterial Cell Cycle We use a systems biology approach to define the complete genetic circuitry that coordinates cell differentiation and cell cycle progression. A cascade of global transcriptional regulators controls the timing of cell cycle events whose expression is coordinated by differential DNA methylation, regulated proteolysis and signaling cascades. The transcriptional circuitry is interwoven with the three-dimensional deployment of key regulatory and morphological proteins.
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Bonnie Bassler
Princeton University, US
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Bonnie Bassler is a member of the National Academy of Sciences and the American Academy of Arts and Sciences. She is a Howard Hughes Medical Institute Investigator and the Squibb Professor of Molecular Biology at Princeton University. The research in her laboratory focuses on the molecular mechanisms that bacteria use for intercellular communication. In 2002, Dr. Bassler was awarded a MacArthur Foundation Fellowship and elected the American Academy of Microbiology. She was made a fellow of the American Association for the Advancement of Science in 2004. She is the 2006 recipient of the American Society for Microbiology’s Eli Lilly Investigator Award for fundamental contributions to microbiological research. In 2008, Bassler was given Princeton University’s President’s Award for Distinguished Teaching. She is the 2009 recipient of the Wiley Prize in Biomedical Science for her paradigm-changing scientific research. Bassler is the President of the American Society for Microbiology. |
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Title & synopsis
Cell-to-Cell Communication in Bacteria
A process called quorum sensing allows bacteria to communicate with one another. Quorum sensing relies on the production, detection, and population-wide response to extracellular signal molecules. Quorum-sensing controlled behaviors are ones that are unproductive when undertaken by an individual bacterium acting alone but become effective when undertaken in unison by the group. For example, quorum sensing controls virulence factor production, biofilm formation, and the exchange of DNA. Thus, quorum sensing is a mechanism that allows bacteria to act as multi-cellular organisms. Current research is focused on developing therapies that interfere with quorum sensing for use as alternatives to traditional antibiotics.
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B. Brett Finlay
University of British Columbia, CA
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B. Brett Finlay is a Professor in the Michael Smith Laboratories, and the Departments of Biochemistry and Molecular Biology, and Microbiology and Immunology at the University of British Columbia, CA. He obtained a B.Sc. (Honors) in Biochemistry at the University of Alberta, where he also did his Ph.D. (1986) in Biochemistry under Dr. William Paranchych, studying F-like plasmid conjugation. His post-doctoral studies were performed with Dr. Stanley Falkow at the Department of Medical Microbiology and Immunology at Stanford University School of Medicine, where he studied Salmonella invasion into host cells. In 1989, he joined UBC as an Assistant Professor in the Biotechnology Laboratory. Dr. Finlay's research interests are focussed on host-pathogen interactions, at the molecular level. By combining cell biology with microbiology, he has been at the forefront of the emerging field called Cellular Microbiology, making several fundamental discoveries in this field, and publishing over 340 papers. His laboratory studies several pathogenic bacteria, with Salmonella and pathogenic E. coli interactions with host cells being the primary focus. He is well recognized internationally for his work, and has won several prestigious awards including the E.W.R. Steacie Prize, the CSM Fisher Scientific Award, CSM Roche Award, a MRC Scientist, five Howard Hughes International Research Scholar Awards, a CIHR Distinguished Investigator, BC Biotech Innovation Award, the Michael Smith Health Research Prize, the IDSA Squibb award, the Jacob Biely Prize, the prestigious Canadian Killam Health Sciences Prize, the Flavelle Medal of the Royal Society, is a Fellow of the Royal Society of Canada and the Canadian Academy of Health Sciences, and is the UBC Peter Wall Distinguished Professor. He is an Officer of the Order of Canada and Order of British Columbia. He is a cofounder of Inimex Pharmaceuticals, Inc., and Director of the SARS Accelerated Vaccine Initiative. He also serves on several editorial and advisory boards, and is a strong supporter of communicating science to the public. |
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Title & synopsis
The role of microbiota in enteric & allergic diseases
The microbiota (normal flora) is comprised of many microbes living in and on our bodies. Only recently have we begun to appreciate the impact of these organisms on our health and disease, impacting on obesity, bowel diseases, type I diabetes, immune development, etc. In developed countries, we have gone to great lengths to minimize our exposure to microbes, both pathogenic and harmless. The Hygiene Hypothesis suggests that perhaps we have gone too far, as hominids have evolved in a sea of microbes, and actually need exposure early in life to microbes to minimize allergic diseases, including asthma. Recent work in our lab has begun to explore the role of the microbiota in experimental asthma and infectious diarrhea. We are finding that the microbiota play central roles in these diseases, and recent results in this area will be discussed, as will their implications in our quest to minimize our exposure to microbes.
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Brain & behaviour
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Cori Bargmann
The Rockefeller University, US
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Cori Bargmann is the Torsten N. Wiesel Professor at the Rockefeller University and an Investigator of the Howard Hughes Medical Institute, US. She received her PhD from MIT, where she worked with Robert A. Weinberg, and pursued postdoctoral studies with H. Robert Horvitz, also at MIT. She joined the faculty of the University of California, San Francisco in 1991 and moved to Rockefeller in 2004. Her lab asks how genes, neural circuits, and experience interact to generate behaviours, using the model animal Caenorhabditis elegans. The lab’s studies identified olfactory signalling mechanisms in this animal and elucidated the underlying logic of olfactory perception and behaviour. By studying genetic variation in the behaviour of wild-type strains, the lab identified a single gene and then a neuronal circuit that controls higher order social behaviours. She is a member of the National Academy of Sciences and the American Academy of Arts and Sciences. She has received the 2009 Richard Lounsbery Award from the US and French National Academies of Sciences, the 2004 Dargut and Milena Kemali International Prize for Research in the Field of Basic and Clinical Neurosciences, the 2000 Charles Judson Herrick Award for comparative neurology, the 1997 Takasago Award for olfaction research and the 1997 W. Alden Spencer Award for neuroscience research.
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Title & synopsis
Genes, environment & decisions: how fixed circuits generate flexible behaviours Which aspects of behaviour are defined by fixed genetic and developmental programmes? How does the brain generate flexible responses to the environment based on context and experience? The nematode C. elegans has a small, genetically hard-wired nervous system, yet its preferences for odours, food sources, and other animals vary based on environmental conditions, internal states, and genetic variation. These factors converge on common neuronal circuits. Analysis of the circuits for flexible behaviours shows that highly detailed wiring diagram of C. elegans is both incomplete and ambiguous, because modulatory inputs that are invisible in the anatomical wiring can fundamentally change the flow of information.
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Florian Engert
Harvard University, US
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Florian Engert is Professor of Molecular and Cellular Biology at Harvard University. The general goal of his laboratory at present and in the intermediate future is the development of the larval zebrafish as a model system for the comprehensive identification and examination of neural circuits controlling visually induced behaviors. To that end he plans to establish and quantify a series of visually induced behaviours and analyze the individual resulting motor components. Using these assays his laboratory will monitor neuronal activity, using genetically encoded and synthetic indicators of neural activity throughout the fish brain in an awake and intact preparation. An extended goal is the study of how changes or variations in the behavior are reflected in changes in the underlying neuronal activity.
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Title & synopsis
Adaptive motorlearning in the zebrafish larva We describe a system in which paralyzed larval zebrafish can navigate a virtual reality environment. We have used this set-up in a series of proof of principle experiments that demonstrate that zebrafish larva can correct for experimentally induced gain changes in the feedback loop in less than a minute. These forms of motor adaptation constitute a robust learning in the zebrafish larva and open the possibility to use functional calcium imaging in these head-fixed preparations to study the underlying changes in the brain before, during and after the training session.
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David J. Anderson
California Institute of Technology, US
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David J. Anderson, PhD, is Seymour Benzer Professor of Biology at the California Institute of Technology and an Investigator of the Howard Hughes Medical Institute. He received an A.B. degree at Harvard and a PhD Degree at Rockefeller University where he trained with Nobelist, Günter Blobel. He performed postdoctoral studies at Columbia University with Nobelist Richard Axel. Awards: Helen Hay Whitney Foundation Fellow, 1983-86; NSF Presidential Young Investigator Award 1986-87; Searle Scholars Award, 1987-88; Alfred P. Sloan research Fellowship in Neuroscience, Javits Investigator in Neuroscience (NIH), 1989-96; Charles Judson Herrick Award in Comparative Neurology, 1990; Ferguson Award for Graduate Teaching, 1994; Ferguson Award for Biology Education, 1996; Ferguson Award for Graduate Teaching, 1998; Alden Spencer Award in Neurobiology, Columbia University, 1999; Elected Associate, The Neurosciences Institute, 2001; American Academy of Arts and Sciences Fellow, 2002; American Association for the Advancement of Science Fellow, 2002; Named Roger W. Sperry Professor of Biology, Caltech, 2004; Alexander von Humboldt Award, 2005; Elected to the National Academies of Sciences, 2007; Named Seymour Benzer Professor of Biology, Caltech, 2009; Named Allen Institute Distinguished Investigator, 2010.
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Title & synopsis
Genetic dissection of emotion circuits in flies & mice This presentation will discuss recent progress towards dissecting neural circuits underlying emotional behaviours related to fear, anxiety and aggression, in both flies and mice.
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Edvard Moser
Norwegian University of Science & Technology, NO
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Edvard Moser is the Director of the Kavli Institute for Systems Neuroscience and the Centre for the Biology of Memory at the Norwegian University of Science and Technology. Together with May-Britt Moser, he has since their group was established in 1996 studied how spatial location and spatial memory are computed in the brain. Their most noteworthy contribution is probably the discovery of grid cells in the entorhinal cortex in 2005, which points to the entorhinal cortex as a hub for the brain network that makes us find our way. They have shown how a variety of functional cell types in the entorhinal microcircuit contribute to representation of self-location, how the outputs of the circuit are used by memory networks in the hippocampus, and how episodic memories are separated from each other in the early stages of the hippocampal memory storage. Edvard Moser is a member of the Board of Reviewing Editors in Science and co-editor of Current Opinion in Neurobiology. He has been awarded the 2011 Louis-Jeantet Prize for Medicine together with May-Britt Moser and Stefan Jentsch.
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Title & synopsis
Transition dynamics of hippocampal memory retrieval
The ability to recall discrete memories is thought to depend on the formation of attractor states in recurrent neural networks but the dynamics supporting such network transitions, at the subsecond time scale, is poorly understood. Using a recently developed ‘teleportation’ protocol, I will show that instantaneous transformation of spatial context generates competitive flickering between pre-formed memory representations in hippocampal cell ensembles, often with complete replacement of active ensembles from one theta cycle to the next. The data provide evidence for competitive network interactions at the time scale of theta cycles during hippocampal memory retrieval.
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